Abstract: RESULTS: The ddI resistance mutations and their resistance scores based on the derivation set were as follows: M41L (score of 14), T69D (24), D123S (40), T139M (54), I180V (53), M184V (-12), V189I (55), Q207K (37), L210W (25), and T215Y (eight).
Postpartum antiretroviral drug resistance in HIV-1-infected women receiving pregnancy-limited antiretroviral therapy.
Result: Mutations associated with resistance to nucleoside analogues (NAMs) were also more frequent among women exposed only to dual-drug PLAT (M41L, 5.0%; D67N, 5.0%; K70R, 10.0; and T215Y, 5.0%) than in those treated with 3 drugs (M41L, 1.1%; D67N, 1.1%; K70R, 1.1%; L210F, 1.1%; K219Q, 1.1%).
Low-abundance HIV species and their impact on mutational profiles in patients with virological failure on once-daily abacavir/lamivudine/zidovudine and tenofovir.
PMID: 20008905
2010
The Journal of antimicrobial chemotherapy
Result: The T215F variant was much more commonly detected than T215Y.
Discussion: In the as-treated analysis, 1/40 subjects treated with twice-daily abacavir/lamivudine/zidovudine + once-daily tenofovir experienced VF; virus from this subject also selected for M184V + TAMs (D67N, K70E, T215Y and K219E), and the authors noted that this subject had incomplete regimen adherence.
Discussion: In their cross-study comparison, they concluded that this regimen was an efficient treatment strategy in moderately pre-treated patients and that virological success was observed for this regimen in the presence of the M184V mutation and low numbers of TAMs, although the presence of at least two TAMs, especially when the <
N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations.
Introduction: M41L and T215Y) and N348I, which may result in reduced in vivo drug efficacy.
Introduction: N348I also increased tenofovir resistance when combined with M41L, L210W and T215Y (HX/3AZT) by 6.0-fold compared to WT (p= 0.009, n=5) and 3-fold compared to the HX/3AZT strain (p=0.008, n=4).
Introduction: N348I was introduced by site directed mutagenesis into the background of wild-type (WT), K103N, <
Introduction: However, when combined with M41L and T215Y (NL/2AZT), N348I decreased tenofovir susceptibility by 1.7-fold (p=0.014, n=4) compared to WT.
Abstract: The most frequent mutations were T215A/Y for NRTIs and K103N/T for NNRTIs.
N348I in reverse transcriptase provides a genetic pathway for HIV-1 to select thymidine analogue mutations and mutations antagonistic to thymidine analogue mutations.
Result: However, in viruses that contained both K70R and T215Y (EC50 = 0.94 +- 0.13 microM, n = 5; 4.1-fold AZT resistance; p = 0.009), the introduction of the N348I mutation clearly compensated for the antagonism of the AZT-resistance phenotype by Y181C: the EC50 value for inhibition of replication of K70R/T215Y/Y181C/N348I HIV-1 by AZT (1.3 +- 0.5 microM, n = 4) was increased 2.8-fold relative to the K70R/T215Y/Y181C virus (EC50 = 0.46 +- 0.14 microM, n = 5; p = 0.032).
Short communication: selection of thymidine analogue resistance mutational patterns in children infected from a common HIV type 1 subtype G source.
PMID: 20334563
2010
AIDS research and human retroviruses
Abstract: At first sampling date, the T215Y-linked pattern was observed in five cases and the T215F cluster was seen in nine.
Abstract: In HIV-1, thymidine analogue mutations (TAMs) cluster in one of two groups (215Y, 41L, 210W, or 215F, 219E/Q), representing two independent mutational patterns (T215Y and T215F cluster, respectively).
Abstract: The mutation T215Y reverted in three out of four patients who discontinued AZT/d4T treatment.
Abstract: Under AZT/d4T therapies, an association was found between the HLA B*13 (in combination with HLA DRB1*0701) and the mutation T215Y.
Abstract: We speculate that in the context of these subtype G viruses, the development of the T215Y mutation may be strongly disfavored whereas the p
Impact of low abundance HIV variants on response to ritonavir-boosted atazanavir or fosamprenavir given once daily with tenofovir/emtricitabine in antiretroviral-naive HIV-infected patients.
PMID: 20380480
2010
AIDS research and human retroviruses
Abstract: In the four FPV/r-treated VFs, baseline HIV TAMs combinations and/or PI mutations were detected in one by PG at VF (RT: L210W + T215C; PR: M46I + L76V) and three others by CA alone (RT: L210W + T215Y; RT: M41L; RT: K65R + K70R; PR: I47V); all four had study drug-associated mutations (CA detecting more HIV-1 resistance mut
The non-nucleoside reverse transcriptase inhibitor efavirenz stimulates replication of human immunodeficiency virus type 1 harboring certain non-nucleoside resistance mutations.
Abstract: Addition of the nucleoside resistance mutations L74V or M41L+T215Y to K101E+G190S improved fitness and abolished EFV-dependent stimulation of replication.
Abstract: D10, a clinical RT backbone containing M41L+T215Y and K101E+G190S, also demonstrated EFV-dependent stimulation that was dependent on the presence of K101E.
Method: Mutagenic primers were as follows: L74V, 5'-CAG TAC TAA ATG GAG AAA AGT AGT AGA TTT CAG AGA AC3' (forward) and 5' GTT CTC TGA AAT CTA CTA CTT TTC TCC ATT TAG TAC TG 3' (reverse);
[Evolution of HIV-1 drug resistance in patients failing combination antiretroviral therapy].
HIV mutation literature information.
PMID: 
2010
AIDS (London, England)
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